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Biomedical subjects

J D Miller

Publications and source records attributed to J D Miller.

At least 127 records · Page 7Linked to original sources
PubMed1995

A formant bandwidth estimation procedure for vowel synthesis [43.72.Ja].

The specification of vowel formant bandwidths for speech synthesis has been inconsistent in the past, perhaps due to the difficulty of measuring formant bandwidths in natural speech and the possible perceptual insignificance of formant bandwidths on the intelligibility of synthetic speech. Here, regression equations are presented for the estimation of formant bandwidths based on measurements from natural speech which is based only on formant center frequency and independent of other formant values. Current usage, as well as comparison with another well-known estimation algorithm suggests that the new procedure should be quite acceptable for some types of speech synthesis.

Female↗
PubMed1995

The evaluation of the wave-form analysis capability of a new strain-gauge intracranial pressure MicroSensor.

Both laboratory and clinical trials have indicated the reliability of a new catheter-tip, strain-gauge intracranial pressure transducer. We report on the results of bench tests comparing the wave-form analysis capabilities of the new Codman intracranial pressure MicroSensor and a similar strain-gauge transducer. Good agreement was found between the two sensors with no significant nonlinearity or hysteresis over a measured pressure range from 0 to 100 mg Hg. Under "fluid-filled" conditions, the MicroSensor showed good reproduction of an arterial pressure wave form; when spectral analysis was used to analyze the two sensor types and break them down into harmonic components, no significant differences could be found for any of the first 10 amplitude and phase harmonics. If proven to stay robust after long-term clinical use, this sensor may be a useful alternative to the existing transducer systems for routinely monitoring the intracranial pressure and its wave form.

Catheters, Indwelling↗
PubMed1995

The adverse drug reaction: a clinical opportunity for pharmacists.

A program is presented that gives the pharmacist the clinical opportunity to assess and evaluate adverse drug reactions in the hospital setting. An adverse drug reaction protocol is discussed that addresses reporting and patient care issues. The pharmacist performs adverse drug reaction assessment at the patient bedside as part of a multidisciplinary team consisting of the pharmacist, nurse, and physician. The protocol provides a method of concurrent adverse drug reaction monitoring and involves the patient in the reporting process.

Adverse Drug Reaction Reporting Systems↗
PubMed1994

Growth cone collapse and neurite retraction from cultured Helisoma neurons in response to antibody Fab fragments against an extracellular matrix protein.

Helisoma neurons require a factor(s) present in conditioned medium (CM), for successful neurite outgrowth in vitro. A approximately 300 kDa Helisoma extracellular matrix (ECM) protein has been identified in CM and is necessary for neurite initiation. Here we show that purified approximately 300 kDa ECM protein supports outgrowth. Furthermore, anti- approximately 300 kDa Fab fragments cause a rapid, dose-dependent decrease in outgrowth when added to neurons already growing in CM, culminating in growth cone collapse and neurite retraction at 200 micrograms/ml. Collapsing growth cones rapidly lost lamellipodia and filopodia transformed into long filamentous strands. Contortion of microtubules in retracting neurites into serpentine shapes, apparently by compressive forces, suggests that large-scale microtubule depolymerization is not a prerequisite for growth cone retraction. These results imply that substrate-bound approximately 300 kDa CM protein is necessary and sufficient for CM-stimulated growth cone initiation and neurite elongation from Helisoma neurons.

Animals↗
PubMed1994

Serotonergic phase advances of the mammalian circadian clock involve protein kinase A and K+ channel opening.

The mammalian circadian clock located in the suprachiasmatic nuclei (SCN) continues to oscillate when isolated in a brain slice preparation, and can be phase shifted in vitro by a variety of serotonergic (5-HTergic) agents. We have previously shown that 5-HT and a 5-HT agonist, quipazine, induce phase advances in the daytime and phase delays at night; the phase advances are mimicked by the 5-HT1A-selective agonist 8-OH-DPAT, by analogs of cyclic AMP, and by treatments that increase endogenous levels of cyclic AMP. Here we investigated the intracellular pathway through which these daytime phase advances occur. We find that quipazine- and 8-OH-DPAT-induced phase advances are blocked by two inhibitors of the cyclic AMP-dependent protein kinase, PK-A (H8 and Rp-cAMPS) as well as by a variety of K+ channel blockers (BaCl2, apamin, and charybdotoxin). Furthermore, we confirm previous work showing that a cyclic AMP analog induces phase advances in the daytime, and show that these phase advances are also blocked by BaCl2 and apamin. Finally, we show that a K+ ionophore induces similar phase advances in the subjective day, and these phase advances are blocked by Rp-cAMPS. These results indicate that both activation of PK-A and opening of K+ channels are necessary for 5-HT-induced phase advances of the SCN circadian clock. We propose a model that can account for our results.

Animals↗
PubMed1994

A possible glial role in the mammalian circadian clock.

The primary mammalian circadian clock is located within the suprachiasmatic nuclei (SCN), but the cellular organization of the clock is not yet known. We investigated the potential role of glial cells in the clock mechanism by determining whether disrupting glial activity affects the in vitro circadian rhythm of neuronal activity and the in vivo circadian activity rhythm in rats. We used two agents (octanol and halothane) that block gap junctions, and one (fluorocitrate) that inhibits glial metabolism. All three agents disrupted the circadian pattern of neuronal activity. Octanol flattened the rhythm at the highest concentration (200 microM) and induced a small phase delay at a lower concentration (66 microM). Halothane and fluorocitrate induced ultradian rhythmicity. Fluorocitrate injected into the SCN of an intact rat induced arrhythmicity for about 1 week, after which the rhythm reappeared with a 1.6 h delay. These results suggest that glia play an important role in the SCN circadian clock.

1-Octanol↗
PubMed1994

Interaction of E. coli Ffh/4.5S ribonucleoprotein and FtsY mimics that of mammalian signal recognition particle and its receptor.

The mechanism of protein translocation across the endoplasmic reticulum membrane of eukaryotic cells and the plasma membrane of prokaryotic cells are thought to be evolutionarily related. Protein targeting to the eukaryotic translocation apparatus is mediated by the signal recognition particle (SRP), a cytosolic ribonucleoprotein, and the SRP receptor, an endoplasmic reticulum membrane protein. During targeting, the 54K SRP subunit (M(r) 54,000; SRP54), a GTP-binding protein, binds to signal sequences and then interacts with the alpha-subunit of the SRP receptor (SR alpha), another GTP-binding protein. Two proteins from Escherichia coli, Ffh and FTsY, structurally resemble SRP54 and SR alpha. Like SRP54, Ffh is a subunit of a cytosolic ribonucleoprotein that also contains the E. coli 4.5S RNA. Although there is genetic and biochemical evidence that the E. coli Ffh/4.5S ribonucleoprotein has an SRP-like function, there is no evidence for an SR alpha-like role for FtsY. Here we show that the Ffh/4.5S ribonucleoprotein binds tightly to FtsY in a GTP-dependent manner. This interaction results in the stimulation of GTP hydrolysis which can be inhibited by synthetic signal peptides. These properties mimic those of mammalian SRP and its receptor, suggesting that the E. coli Ffh/4.5S ribonucleoprotein and FtsY have functions in protein targeting that are similar to those of their mammalian counterparts.

Amino Acid Sequence↗
PubMed1994

Pharmacokinetic fate and pathological effects of 14C-fumonisin B1 in laying hens.

Presence of fumonisin B1 (FB1), a major metabolite of Fusarium moniliforme, in corn is of great concern to both human and animal health because of its wide range of toxicity. The pharmacokinetics of FB1 was studied in laying hens following oral and intravenous administration of 14C-labelled FB1. After iv dosing (2.0 mg = 23.68 kBq/kg bw) plasma radioactivity underwent a very rapid bi-exponential decline (t1/2 alpha = 2.5 +/- 0.3 min; t1/2 beta = 48.8 +/- 11.2 min) with negligible levels measured after 4-6 hr. Mean value for the apparent volume of distribution at steady state (Vdss) was 18.27 ml/kg, apparent volume of central compartment (Vd beta) was 82.20 ml/kg and plasma clearance was 1.18 ml/min/kg. At 24 hr post-dosing only trace residues were present in liver, kidney, and cecum. When dosed by the oral route (2.0 mg = 47.36 kBq/kg bw), systemic absorption of fumonisin appeared to be poor (F = 0.71 +/- 0.5%) with peak plasma concentrations of only 40-145 dpm/ml (equivalent to 28-103 ng FB1 and/or metabolites per ml) between 1.5 and 2.5 hr. At 24 hr post-dosing only trace amounts were present in crop, liver, kidney, small intestine, and cecum. In both orally and iv dosed birds almost all (97.7 +/- 3.73%) of the radioactivity was recovered in excreta by the end of the 24 hr experiment period and no residues were found in eggs laid during the 24 hr post-dosing period.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1994

Secondary metabolites of Penicillium bilaii strain PB-50.

A phosphate-solubilizing strain of Penicillium bilaii was tested for the production of gliotoxin and other toxic compounds. The strain was fermented under five different conditions to allow the expression of various metabolites, including gliotoxin. These included Czapek-yeast extract medium under both shaken and still conditions as well as Czapek-yeast extract/malt extract/peptone medium and sucrose/glycerol medium in shake flasks. In addition, culture filtrate from an industrial fermentation of the fungus was examined. No gliotoxin was produced in any of the media. No other expected P. bilaii metabolites were found. Three compounds were identified in all samples: dibutyl phthalate, 1-(4-hydroxy-phenyl)ethanone and 4-hydroxy-3,6-dimethyl-2H-pyran-2-one. The production of other metabolites was dependent on the culture conditions. Two hyalodendrin derivatives were found in some fermentations and two related compounds were tentatively identified. None of the compounds found have been reported as toxic. The identity of the culture was confirmed by comparison with the ex-type culture of P. bilaii.

Acetophenones↗
PubMed1994

Cause, distribution and significance of episodes of reduced cerebral perfusion pressure following head injury.

A group of 74 patients with head injury (54 severe, 17 moderate and 3 minor) had continuous monitoring of both arterial and intracranial pressure with computer-based registration of these pressures, cerebral perfusion pressure and other variables. In 60 patients cerebral perfusion pressure CPP fell below 60 mm Hg for periods of 5 minutes or longer. The distribution over time of these reductions in CPP during up to 12 days of monitoring was studied, and each episode of reduced CPP was attributed to a fall in arterial pressure, an increase in intracranial pressure, or both. Two clusters of reduced CPP were found, one during the first 24 hours of monitoring, when reduced CPP was mainly caused by a reduction in arterial pressure, and the other at 5 or 6 days after injury, when reduced CPP was due mainly to an increase in intracranial pressure. There was a significant correlation between low CPP due to reduced arterial pressure and the Injury Severity Score (p < 0.001), suggesting that resuscitative measures may have been less than optimal in these cases. There was also significant correlation between the duration of low CPP and low arterial pressure and an adverse outcome from injury as assessed at 6, 12 and 24 months after injury (p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Chemical treatment of carpets to reduce allergen: a detailed study of the effects of tannic acid on indoor allergens.

Tannic acid (TA), a protein-denaturing agent, has been reported to reduce allergen levels in house dust and is marketed for that purpose as 1% and 3% solutions. We investigated the effects of TA on dust allergens by using monoclonal antibody-based ELISAs for mite (Der p I, Der f I, and group II) and cat (Fel d I) allergens. Initial studies confirmed that TA reduced allergen levels in carpet dust. However, when dust samples from treated carpets are extracted in saline solution, residual TA redissolves and may interfere with the assessment of allergens. In the laboratory, concentrations of TA as low as 0.1% inhibited the assays, but this effect may be prevented by addition of 5% bovine serum albumin (BSA). After treatment of dust samples in the laboratory with 3% TA, the apparent reductions in Der p I and Der f I levels were 89% and 96%, respectively, but when the samples were extracted in 5% BSA the reductions were 74% and 92%. Similar effects were seen with dust samples from carpets treated with TA. In an extreme case in which a carpet had been repeatedly treated with TA, the apparent concentration of Der p I was < 0.05 microgram/gm without BSA and 2.1 and 8.4 microgram/gm when extracted in the presence of 1% and 5% BSA, respectively. Our testing of the ability of TA to denature Fel d I demonstrated an 80% reduction in allergen, but only in samples with an initial concentration of less than 200 micrograms Fel d I/gm dust.(ABSTRACT TRUNCATED AT 250 WORDS)

Air Pollution, Indoor↗
PubMed1994

Chloride channel block phase advances the single-unit activity rhythm in the SCN.

The mammalian suprachiasmatic nuclei (SCN) contain a circadian pacemaker that exhibits a 24 h rhythm in single-unit activity in vivo and in vitro. Chloride channel block by a saturating concentration of picrotoxin at either CT6 or CT15 produces large phase advances in the SCN single-unit activity rhythm in vitro. These phase advances are not affected by simultaneous blockade of voltage-sensitive sodium and calcium channels by TTX and magnesium. Thus, the effects of picrotoxin appear to be mediated by direct blockade of the chloride channel, rather than subsequent membrane depolarization. GABA-A receptor-mediated chloride flux may be part of the mechanism of circadian timekeeping.

Action Potentials↗